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Commentary 10.1172/JCI132441

Regulating heart repair with cardiac-specific T lymphocytes

Ziad Mallat

Department of Medicine, Division of Cardiovascular Medicine, University of Cambridge, Cambridge, United Kingdom.

Address correspondence to: Ziad Mallat, Department of Medicine, University of Cambridge, Addenbrookes Hospital, Hills Road, Cambridge CB2 0QQ, United Kingdom. Email: zm255@medschl.cam.ac.uk.

Find articles by Mallat, Z. in: JCI | PubMed | Google Scholar |

First published October 14, 2019 - More info

Published in Volume 129, Issue 11 on November 1, 2019
J Clin Invest. 2019;129(11):4587–4589. https://doi.org/10.1172/JCI132441.
© 2019 American Society for Clinical Investigation
First published October 14, 2019 - Version history

Cardiac tissue necrosis secondary to coronary artery occlusion is one of the most common and deadly sterile injuries in developed countries. In this issue of the JCI, Rieckmann et al. identified and characterized antigen-specific CD4+ T helper (Th) cells that developed in the context of myocardial infarction (MI) in mice. They showed that myosin heavy chain α (MYHCA) is a dominant cardiac autoantigen and that T cells with T cell receptor (TCR) specificity to MYHCA acquired a Treg phenotype when adoptively transferred into infarcted mice, which mediated a cardioprotective healing response. Thus, Rieckmann et al. showed that an acute ischemic insult to the heart, which induces sterile inflammation, promoted, rather than limited, protective T cell autoimmunity. Notably, strategies that support an antigen-specific Treg response may limit the immune-inflammatory response and promote cardiac repair after acute MI.

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